卡托普利对心动过速心肌病心肌缝隙连接蛋白重构的影响

目的研究卡托普利对心动过速心肌病（tachycardia induced cardiomyopathy, TIC）实验犬心室肌中缝隙连接蛋白重构的影响。方法24只犬随机分为3组。起搏组：实验犬植入永久起搏器，经颈外静脉途径将起搏电极导线置入右心耳(起搏频率350～450次／min)。起搏加药物组：起搏器植入同起搏组，起搏器植入前3?d至起搏8周后，每日给予卡托普利50mg 2次／日口服；对照组：实验犬未植入起搏器也未服药。分别在起搏前及起搏后第1、4、8周记录12导联心电图并行超声心动图检查，起搏8周后行心导管检查，并用激光共聚焦显微镜测定3组左心室肌缝隙连接蛋白（Connexin43, Cx43）含量。结果左心室肌Cx43含量比较：起搏组vs对照组（P＜0.001）；起搏组vs起搏加药物组（P＜0.05），起搏组Cx43含量均明显减低。结论卡托普利有明显延缓慢性实验犬TIC左心室Cx43下降的趋势。

Effect of Captopril on myocardium gap junction remodeling during tachycardia-induced cardiomyopathy

To investigate the effects of Captopril on left ventricular connexin remodeling during tachycardia induced cardiomyopathy in canines. Methods Twenty-four dogs were randomly divided into 3 groups. In the pacing group, each dog was implanted with a permanent pacemaker (pacing at 350-450 bpm), the pacing electrode was implanted in the right atrial appendage through the external jugular vein. In the pacing and drug group, each dog was given Captopril 50mg twice a day three days before the pacemaker was implanted and through out the study. The pacing procedure was the same as in the pacing group. In the control group, no pacemakers or drugs were given. Before pacing and 1,4,8 weeks after pacing, the echocardiography and ECG were measured, and also the heart function was measured. After 8 weeks′ pacing, catheterization was used to assess the systolic and diastolic functions and the content of Cx43 was determined by confocal immunofluoroscopy. ResultsThe content of Cx43 was significantly different between the pacing group and the control group（P＜0.001）and between the pacing group and the pacing and drug group（P＜0.05）. Conclusions Captopril may prevent the decrease of the content of Cx43， and prevents gap junction remodeling in dogs with long-term rapid atrial pacing．